z-logo
open-access-imgOpen Access
Modulation of Type 1 Diabetes Susceptibility by Tumor Necrosis Factor Alpha −308 G/A and Lymphotoxin Alpha +249 A/G Haplotypes and Lack of Linkage Disequilibrium with Predisposing DQB1-DRB1 Haplotypes in Bahraini Patients
Author(s) -
Mouna Stayoussef,
Fayza A. Al-Jenaidi,
Abduljabbar Al-Abbasi,
Khadija AlOla,
Haya Khayyat,
Touhami Mahjoub,
Wassim Y. Almawi
Publication year - 2007
Publication title -
clinical and vaccine immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.649
H-Index - 77
eISSN - 1556-6811
pISSN - 1556-679X
DOI - 10.1128/cvi.00410-07
Subject(s) - lymphotoxin alpha , haplotype , linkage disequilibrium , lymphotoxin , alpha (finance) , tumor necrosis factor alpha , linkage (software) , genetics , biology , beta (programming language) , type 2 diabetes , immunology , allele , endocrinology , diabetes mellitus , medicine , gene , computer science , patient satisfaction , programming language , construct validity , nursing
Tumor necrosis factor alpha (TNF-α) −308 G/A and lymphotoxin alpha (LTα) +249 A/G single-nucleotide polymorphisms were investigated in 228 type 1 diabetes mellitus (T1DM) patients and 240 controls. Only LTα +249G allele and +249G/+249G genotype frequencies were higher among patients, and no linkage disequilibrium was found between TNF-α/LTα alleles and susceptible/protectiveDRB1-DQB1 haplotypes. TNF-α/LTα T1DM-susceptible (−308G/+249G) and protective (−308G/+249A) haplotypes were identified.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom